Elevated concentrations of leukotriene D4 in pulmonary edema fluid of patients with the adult respiratory distress syndrome

The possible contribution of metabolites of arachidonic acid to the increased permeability of the alveolar-capillary barrier in the adult respiratory distress syndrome was examined by quantifying the pulmonary edema fluid concentrations of lipoxygenase and cyclooxygenase products. The concentration of leukotriene D₄ in pulmonary edema fluid of 10 patients with the adult respiratory distress syndrome (18.5±6.8 pmol/ml; mean±SD), assessed by specific radioimmunoassay after isolation of the mediator, was significantly higher (P<0.001) than that of five patients with cardiogenic pulmonary edema (4.4±1.1 pmol/ml). The concentrations of leukotrienes B₄ and C₄, prostaglandin E₂, and thromboxane B₂ in edema fluid were not significantly different in the adult respiratory distress syndrome patients than in the other subjects with pulmonary edema. The edema fluid concentration of leukotriene D₄ correlated with the ratio of edema fluid to plasma concentrations of albumin (r=0.64). Leukotriene D₄ thus may contribute to the permeability defect which allows an accumulation of proteinrich alveolar fluid in the adult respiratory distress syndrome.This work was supported in part by Grants HL31809, HL25816, HL19155, and AI19784 from the National Institutes of Health.     

Neuropeptides in pulmonary edema fluid of adult respiratory distress syndrome

A role for peptidergic nerves in the adult respiratory distress syndrome (ARDS) was examined by radioimmunochemically quantifying neuropeptides in pulmonary edema (PE) fluids from seven patients with ARDS and six patients with PE from congestive heart failure (CHF). The PE fluid mean concentrations of substance P (SP) and gastrin-releasing peptide (GRP) were significantly higher in ARDS (0.59 ±0.29SD and 0.10=0.03 nM, respectively,P < 0.001 for both) than in CHF (0.19±0.08 and 0.04±0.01), whereas no difference was detected between the mean levels of vasoacti ve intestinal peptide (VIP) and calcitonin gene-related peptide (CGRP) in the two forms of PE. Mean alveolar fluid concentration of SP was 8.7 nM (range 2.1–20.5 nM,N=4) in sheep with acute lung injury from intravenousPseudomonas aeruginosa, but was undetectable in sheep with balloon-induced high left atrial pressure simulating CHF (N=2) or control sheep (N=2). Pulmonary lymphatic clearance of SP, which reflected the rate of generation of SP in the lungs, attained a maximum of 25–95 pmol/h in sheep givenP. aeruginosa intravenously, but was detected in only one of four control sheep at a lower level. Some pulmonary neuropeptides thus are released locally by acute lung injury and may contribute to endothelial and/or epithelial abnormalities underlying the altered capillary-alveolar permeability in ARDS.     

The adult respiratory distress syndrome

Summary The adult respiratory distress syndrome is a condition of life-threatening organ failure triggered by blood-borne factors and challenges which arrive via the airways. Vascular damage is a necessary, but often not sufficient criterion for ARDS, which is observed in an acute and chronic form. There is a consensus that neutrophils and their products contribute to the pathogenesis of the syndrome, and that lung vascular tone regulation and endothelial and epithelial cell permeability are affected in ARDS. Whereas the precise roles of individual mediators for the development of ARDS are still ill-defined, a synergism between lipid mediators and other injurious principles is recognized. Chronic ARDS is a proliferative disorder which may require different treatment strategies than acute ARDS. Specific treatment modalities which inhibit the interaction between activated neutrophils and the lung endothelium, and surfactant replacement might have a future as early therapy approaches.Abbreviations ARDS Adult respiratory distress syndrome - BALF Bronchoalveolar lavage fluid - EDRF Endothelium-dependent relaxing factor - IL1 Interleukin 1 - PAF Platelet-activating factor - PDGF Platelet-derived growth factor - TNF Tumor necrosis factor A tribute to Thomas L. Petty who originally described ARDS, to his many important contributions as one of the founders of Modern Clinical Pulmonary Medicine, and his many years of inspirational leadership at the University of Colorado Health Sciences Center     

Pulmonary circulation in embolic pulmonary edema

Laboratory of Pathophysiology of Respiration and Bioengineering Laboratory, Research Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. Department of Pathological Physiology, Yaroslavl' Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR B. I. Tkachenko.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 107, No. 2, pp. 157–161, February, 1989.     

Pathogenesis of pulmonary edema: learning from high-altitude pulmonary edema

Pulmonary edema is a problem of major clinical importance resulting from a persistent imbalance between forces that drive water into the airspace of the lung and the biological mechanisms for its removal. Here, we will review the fundamental mechanisms implicated in the regulation of alveolar fluid homeostasis. We will then describe the perturbations of pulmonary fluid homeostasis implicated in the pathogenesis of pulmonary edema in conditions associated with increased pulmonary capillary pressure, namely cardiogenic pulmonary edema and high-altitude pulmonary edema (HAPE), with particular emphasis on the latter that has provided important new insight into underlying mechanisms of pulmonary edema. We will provide evidence that impaired pulmonary endothelial and epithelial nitric oxide synthesis and/or bioavailability may represent a central underlying defect predisposing to exaggerated hypoxic pulmonary vasoconstriction, and, in turn, capillary stress failure and alveolar fluid flooding. We will then demonstrate that exaggerated pulmonary hypertension, while possibly a prerequisite, may not always be sufficient to cause HAPE, and how defective alveolar fluid clearance may represent a second important pathogenic mechanism. Finally, we will outline, how this new insight gained from studies in HAPE, may be translated into the management of pulmonary edema and hypoxemia related disease states in general.     

High-dose corticosteroids in patients with the adult respiratory distress syndrome

Corticosteroids are widely used as therapy for the adult respiratory distress syndrome (ARDS) without proof of efficacy. We conducted a prospective, randomized, double-blind, placebo-controlled trial of methylprednisolone therapy in 99 patients with refractory hypoxemia, diffuse bilateral infiltrates on chest radiography and absence of congestive heart failure documented by pulmonary-artery catheterization. The causes of ARDS included sepsis (27 percent), aspiration pneumonia (18 percent), pancreatitis (4 percent), shock (2 percent), fat emboli (1 percent), and miscellaneous causes or more than one cause (42 percent). Fifty patients received methylprednisolone (30 mg per kilogram of body weight every six hours for 24 hours), and 49 received placebo according to the same schedule. Serial measurements were made of pulmonary shunting, the ratio of partial pressure of arterial oxygen to partial pressure of alveolar oxygen, the chest radiograph severity score, total thoracic compliance, and pulmonary-artery pressure. We observed no statistical differences between groups in these characteristics upon entry or during the five days after entry. Forty-five days after entry there were no differences between the methylprednisolone and placebo groups in mortality (respectively, 30 of 50 [60 percent; 95 percent confidence interval, 46 to 74] and 31 of 49 [63 percent; 95 percent confidence interval, 49 to 77]; P = 0.74) or in the reversal of ARDS (18 of 50 [36 percent] vs. 19 of 49 [39 percent]; P = 0.77). However, the relatively wide confidence intervals in the mortality data make it impossible to exclude a small effect of treatment. Infectious complications were similar in the methylprednisolone group (8 of 50 [16 percent]) and the placebo group (5 of 49 [10 percent]; P = 0.60). Our data suggest that in patients with established ARDS due to sepsis, aspiration, or a mixed cause, high-dose methylprednisolone does not affect outcome.     

Alveolar surfactant and adult respiratory distress syndrome

Summary The adult respiratory distress syndrome (ARDS) is characterized by extended inflammatory processes in the lung microvascular, interstitial, and alveolar compartments, resulting in vasomotor disturbances, plasma leakage, cell injury, and complex gas exchange disturbances. Abnormalities in the alveolar surfactant system have long been implicated in the pathogenetic sequelae of this life-threatening syndrome. This hypothesis is supported by similarities in pulmonary failure between patients with ARDS and preterm babies with infant respiratory distress syndrome, known to be triggered primarily by lack of surfactant material. Mechanisms of surfactant alterations in ARDS include: (a) lack of surface-active compounds (phospholipids, apoproteins) due to reduced generation/release by diseased pneumocytes or to increased loss of material (this feature includes changes in the relative composition of the surfactant phospholipid and/or apoprotein profiles); (b) inhibition of surfactant function by plasma protein leakage (inhibitory potencies of different plasma proteins have been defined); (c) incorporation of surfactant phospholipids and apoproteins into polymerizing fibrin upon hyaline membrane formation; and (d) damage/inhibition of surfactant compounds by inflammatory mediators (proteases, oxidants, nonsurfactant lipids). Alterations in alveolar surfactant function may well contribute to a variety of pathophysiological key events encountered in ARDS. These include decrease in compliance, ventilation-perfusion mismatch including shunt flow due to altered gas flow distribution (atelectasis, partial alveolar collapse, small airway collapse), and lung edema formation. Moreover, more speculative at the present time, surfactant abnormalities may add to a reduction in alveolar host defense competence and an upregulation of inflammatory events under conditions of ARDS. Persistent atelectasis of surfactant-deficient and in particular fibrin-loaded alveoli may represent a key event to trigger fibroblast proliferation and fibrosis in late ARDS (collapse induration). Overall, the presently available data on surfactant abnormalities in ARDS lend credit to therapeutic trials with transbronchial surfactant administration. In addition to the classical goals of replacement therapy defined for preterm infants (rapid improvement in lung compliance and gas exchange), this approach will have to consider its impact on host defense competence and inflammatory and proliferative processes when applied in adults with respiratory failure.Abbreviations ARDS adult respiratory distress syndrome - IRDS infant respiratory distrss syndrome - PC phosphatidylcholine - PG phosphatidylglycerol - PE phosphatidylethanolamine - PS phosphatidylserine - PI phosphatidylinositol - Sph spingomyelin - BAL bronchoalveolar lavage - TNF tumor necrosis factor Dedicated to Prof. Dr. N. Zöllner on the occasion of his 70th birthday     

A practical approach to adult acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) is a common disease encountered in hospitalized adult patients that, historically, has carried a very high mortality. This article reviews the clinical features and how pathophysiology informs the evidence-based management of ARDS.     

The pulmonary vascular lesions of the adult respiratory distress syndrome

Specimen arteriography, morphometry, and light and electron microscopy were used for examination of the pulmonary vasculature of 22 patients who died with the adult respiratory distress syndrome (ARDS), for the purpose of defining the lesions that contribute to pulmonary hypertension in this setting. The different lesions correlated with the duration rather than the cause of ARDS. Thromboemboli occurred in 21 patients, and macrothrombi found at autopsy correlated with the number of filling defects on antemortem angiography. Acute endothelial injury was documented ultrastructurally even in intermediate and late-stage patients. Fibrocellular intimal obliteration of arteries, veins, and lymphatics and infective vasculitis were prominent in those surviving beyond 10 days. In long-term survivors, tortuous arteries and irregularly dilated capillaries were striking features. Peripheral extension of vascular smooth muscle and a significant increase in the percentage of medial thickness of muscular arteries with duration of ARDS were noted. The pathogenesis and clinical significance of these lesions is discussed.     

Effect of irradiation on the formation of hemodynamic pulmonary edema

Experiments on 233 albino rats showed that large doses of ionizing radiation, causing marked leukopenia, increased the resistance of animals to pulmonary edema under the influence of adrenalin. This effect was particularly marked on the fourth day after irradiation. Relatively small doses (under 100R) and also irradiation separately of the head, thorax, or abdomen, on the other hand facilitated the development of pulmonary edema.Department of Pathological Physiology, Yaroslavl' Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Fedorov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 86, No. 9, pp. 280–282, September, 1978.     

肺血管内皮细胞分泌功能的改变与急性肺损伤/急性呼吸窘迫综合征

急性肺损伤(acute lung injury,ALI)/急性呼吸窘迫综合征(acute respiratory distress syndrome, ARDS)是临床上常见的急危重症,病死率高达25%~45%,治疗上主要限于器官功能与全身支持治疗,尤其是呼吸支持治疗,“等待”肺损伤的缓解。在ARDS发病机制中肺血管内皮细胞(pulmonary vascular endothelial cell,PVEC)既是受损的主要靶细胞,更是活跃的炎症和效应细胞,血管内皮细胞(vascular endothelial cell,VEC)的激活和损伤程度与ARDS预后密切相关。本文将主要阐述ALI/ARDS发病机制中PVEC部分分泌功能的改变。     

Reactive type II pneumocytes in bronchoalveolar lavage fluid from adult respiratory distress syndrome can be mistaken for cells of adenocarcinoma

A growing body of literature illustrates that bronchoalveolar lavage is a reliable and efficient means of diagnosing primary and secondary malignancies in the lung. Its safety in severely compromised patients often makes it preferable to other biopsy procedures. However, a variety of reparative and degenerative pulmonary disorders may result in cytologic alterations so severe that pneumocytes resemble cells of malignancy. We describe four patients with the adult respiratory distress syndrome from whom lavage fluid showed gland-like groups of malignant-appearing cells morphologically consistent with adenocarcinoma. Transbronchial biopsy sections in one case and lavage fluid electron microscopy in another showed that these pseudomalignant cells were reactive Type II pneumocytes with surface microvilli, cell junctions, and numerous cytoplasmic myelin figures. Careful clinicopathologic correlation is the best way to ensure accurate diagnosis in these cases.     

Depressed bronchoalveolar urokinase activity in patients with adult respiratory distress syndrome

Abundant deposition of bronchoalveolar fibrin and fibronectin occurs during the exudative phase of the adult respiratory distress syndrome (ARDS), promoting hyaline-membrane formation and subsequent alveolar fibrosis. To explore the mechanisms that account for the persistence of bronchoalveolar fibrin and fibronectin, we compared the activity of urokinase, which is necessary for plasminogen activation and fibrin degradation, in cell-free bronchoalveolar-lavage fluid from 8 patients with ARDS, 9 patients with acute pulmonary diseases other than ARDS, and 10 normal subjects. The mean level of urokinase activity in the lavage fluid from the patients with ARDS was 0.003 IU per milliliter of fluid (range, 0 to 0.008), which was significantly lower (P = 0.001) than the level in the fluid from either the patients with pulmonary diseases other than ARDS (0.118 IU per milliliter [range, 0.032 to 0.295]) or the normal subjects (0.129 IU per milliliter [range, 0.045 to 0.198]). The lavage fluid from all the patients with ARDS also had antiplasmin activity, which would promote the persistence of fibrin. A true decrease in urokinase activity was confirmed by the failure of the lavage fluid from the patients with ARDS to convert [125I]plasminogen to plasmin. Despite the low urokinase activity, immunochemical assays revealed normal levels of urokinase antigen in the fluid from the patients with ARDS, suggesting the presence of urokinase inhibitors. Inhibitors were demonstrated directly by a fibrin gel-underlay assay that detects complexes of urokinase with inhibitors. Plasminogen-activator inhibitor type 1 was the principal inhibitor identified. We conclude that increased antifibrinolytic activity due to both urokinase inhibitors and antiplasmins in the bronchoalveolar compartment of patients with ARDS contributes to the formation and persistence of hyaline membranes, a key component of alveolar histopathology in ARDS.     

Fas and fas ligand are up-regulated in pulmonary edema fluid and lung tissue of patients with acute lung injury and the acute respiratory distress syndrome

Apoptosis mediated by Fas/Fas ligand (FasL) interaction has been implicated in human disease processes, including pulmonary disorders. However, the role of the Fas/FasL system in acute lung injury (ALI) and in the acute respiratory distress syndrome (ARDS) is poorly defined. Accordingly, we investigated both the soluble and cellular expression of the Fas/FasL system in patients with ALI or ARDS. The major findings are summarized as follows. First, the soluble expression of the Fas/FasL system was assessed in undiluted pulmonary edema fluid and simultaneous plasma. Pulmonary edema fluid obtained from patients with ALI or ARDS (n = 51) had significantly higher concentrations of both soluble Fas (27 ng/ml; median; P < 0.05) and soluble FasL (0.125 ng/ml; P < 0.05) compared to control patients with hydrostatic pulmonary edema (n = 40; soluble Fas, 12 ng/ml; soluble FasL, 0.080 ng/ml). In addition, the concentrations of both soluble Fas and soluble FasL were significantly higher in the pulmonary edema fluid of the patients with ALI or ARDS compared to simultaneous plasma samples (soluble Fas, 16 ng/ml; soluble FasL, 0.058 ng/ml; P < 0.05), indicating local release in the lung. Higher soluble Fas concentrations were associated with worse clinical outcomes. Second, cellular expression of the Fas/FasL system was assessed by semiquantitative immunofluorescence microscopy in lung tissue obtained at autopsy from a different set of patients. Both Fas and FasL were immunolocalized to a greater extent in the patients who died with ALI or ARDS (n = 10) than in the patients who died without pulmonary disease (n = 10). Both proteins were co-expressed by epithelial cells that lined the alveolar walls, as well as by inflammatory cells and sloughed epithelial cells that were located in the air spaces. Semiquantitative immunohistochemistry showed that markers of apoptosis (terminal dUTP nick-end labeling, caspase-3, Bax, and p53) were more prevalent in alveolar wall cells from the patients who died with ALI or ARDS compared to the patients who died without pulmonary disease. These findings indicate that alveolar epithelial injury in humans with ALI or ARDS is in part associated with local up-regulation of the Fas/FasL system and activation of the apoptotic cascade in the epithelial cells that line the alveolar air spaces.     

BiPAP呼吸机治疗慢性阻塞性肺疾病合并Ⅱ型呼吸衰竭30例疗效观察

目的：了解BiPAP呼吸机对治疗慢性阻塞性肺疾病(chronic obstructive pulmonary diseases,COPD)合并Ⅱ型呼吸衰竭患者的疗效。方法：62例COPD合并轻、中度Ⅱ型呼吸衰竭（pH 7.25~7.35）的住院患者随机被分为治疗组（30例）和对照组（32例）,治疗组在常规治疗的基础上连续使用BiPAP呼吸机3 d（2次/d,4 h/次）,对照组仅给以常规治疗。观察两组患者治疗前后血气分析、呼吸频率、心率、Borg评分、肺功能变化以及气管插管率和住院天数。结果：治疗3 d后,治疗组pH和PaCO2的改善较对照组更明显(P＜0. 05)。治疗组气管插管率明显低于对照组（P＜0. 05）; pH 7.31~7.35患者中治疗组气管插管率与对照组类似（P＞0. 05）,pH 7.25~7.30患者中治疗组气管插管率明显低于对照组（P＜0. 01）。治疗组住院天数少于对照组（P＜0. 05）。结论：BiPAP呼吸机能更好地改善COPD合并轻、中度Ⅱ型呼吸衰竭患者的pH和PaCO2,尤其降低中度呼吸衰竭患者气管插管率,缩短住院时间。     

A study on the role of noninvasive ventilation in mild-to-moderate acute respiratory distress syndrome

Aim:There is sparse data on the role of noninvasive ventilation (NIV) in acute respiratory distress syndrome (ARDS) from India. Herein, we report our experience with the use of NIV in mild to moderate ARDS.Results:A total of 41 subjects (27 women, mean age: 30.9 years) were included in the study. Tropical infections followed by abdominal sepsis were the most common causes of ARDS. The use of NIV was successful in 18 (44%) subjects, while 23 subjects required intubation. The median time to intubation was 3 h. Overall, 19 (46.3%) deaths were encountered, all in those requiring invasive ventilation. The mean duration of ventilation was significantly higher in the intubated patients (7.1 vs. 2.6 days, P = 0.004). Univariate analysis revealed a lack of improvement in PaO₂/FiO₂ at 1 h and high baseline Acute Physiology and Chronic Health Evaluation II (APACHE II) as predictors of NIV failure.Conclusions:Use of NIV in mild to moderate ARDS helped in avoiding intubation in about 44% of the subjects. A baseline APACHE II score of >17 and a PaO₂/FiO₂ ratio <150 at 1 h predicts NIV failure.     

Character of the pulmonary circulation in experimental pulmonary edema dated by artificial ventilation

Laboratory of Pathophysiology of Respiration and Bioengineering Laboratory, Research Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR B. B. Moroz.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 109, No. 2, pp. 126–128, February, 1990.     

Prekallikrein activation in the adult respiratory distress syndrome

Prekallikrein is the zymogen form of plasma kallikrein, a proteolytic enzyme of the contact system of blood coagulation, fibrinolysis and kinin formation. To assess whether prekallikrein was activated in the adult respiratory distress syndrome (ARDS), we examined plasma samples from 12 critically ill patients including five individuals with ARDS. Using the ratio between functional prekallikrein and prekallikrein-kallikrein antigen as an index for prekallikrein activation, we found that prekallikrein was extensively activated in patients with ARDS, while this was significantly less in the case of critically ill patients without ARDS. Following activation of prekallikrein in plasma, kallikrein reacts with its substrates and with protease inhibitors, among which the alpha 2-glycoprotein C1-inhibitor. Thus, we examined whether C1-inhibitor of critically ill individuals was modified in a way suggesting that it had reacted with kallikrein. Such a modification was found in the five patients with ARDS, while it was not detectable in the seven patients without ARDS. This observation further confirmed the activation of prekallikrein in patients with ARDS. We suggest that plasma kallikrein-mediated reactions, which include bradykinin release and neutrophil activation, may contribute to the pathogenesis of ARDS.     

Enhanced expression of Fas and FasL modulates apoptosis in the lungs of severe P. falciparum malaria patients with pulmonary edema

Apoptosis mediated by Fas/FasL has been implicated in pulmonary disorders. However, little is known about the relationship between Fas and FasL in the process of lung injury during malaria infection. Paraffin-embedded lung tissues from malaria patients were divided into two groups: those with pulmonary edema (PE) and those without pulmonary edema (non-PE). Normal lung tissues were used as the control group. Cellular expression of Fas, FasL, and the markers of apoptotic caspases, including cleaved caspase-3 and cleaved caspase-8 in the lung tissues were investigated by the immunohistochemistry (IHC) method. Semi-quantitative analysis of IHC staining revealed that cellular expression of Fas, FasL, cleaved caspase-8, and cleaved caspase-3 were significantly increased in the lungs of patients with PE compared with the lungs of patients with non-PE and control groups (all P < 0.05). In addition, significant positive correlations were obtained between Fas and apoptosis (r_s = 0.937, P < 0.001) and FasL and apoptosis (r_s = 0.808, P < 0.001). Significant positive correlations were found between Fas and FasL expression (r_s = 0.827, P < 0.001) and between cleaved caspase-8 and cleaved caspase-3 expression (r_s = 0.823, P < 0.001), which suggests that Fas-dependent initiator and effector caspases, including cleaved caspase-8 and caspase-3, are necessary for inducing apoptosis in the lungs of patients with severe P. falciparum malaria. The Fas/FasL system and downstream activation of caspases are important mediators of apoptosis and may be involved in the pathogenesis of pulmonary edema in severe P. falciparum malaria patients. The proper regulation of the Fas/FasL pathway can be a potential treatment for pulmonary complications in falciparum malaria patients.     

Complement activation and the prognostic value of C3a in patients at risk of adult respiratory distress syndrome

In vivo and in vitro studies have shown that complement activation plays an important role in the pathogenesis of the adult respiratory distress syndrome (ARDS). In a prospective study of polytrauma patients at risk of ARDS (n = 38) complement parameters were determined over a period of 14 days in serial plasma samples (obtained every 6 h during the first 48 h). Polytrauma induced a rapid and remarkable complement activation. Low levels of the complement proteins C3, C4, C1 inhibitor (C1 INH) factor I and factor H during the first 48 h indicated complement consumption in all patients. Elevated C3a levels in the first few hours after injury were associated with the later development of ARDS. A more sensitive indicator than C3a alone was the calculated C3a:C3 ratio discriminating ARDS and non-ARDS patients. A second rise of C3a levels and C3a:C3 ratio from day 4 on paralleled the course of extravascular lung water. To assess the mode of complement activation, the activation-specific protein complexes C1rC1s-C1 INH and C3b(Bb)P were measured in some of the patients. We demonstrate that in the first 48 h complement activation occurred via the alternative pathway only and was later followed by an additional activation via the classical pathway. Our observations suggest that monitoring of C3a and C3 in plasma can identify polytrauma patients at high risk for ARDS at an early stage of the disease.